The pathogenic fungus Cryphonectria parasitica (formerly Endothia parasitica) is a member of the Ascomycota (sac fungi) taxon, and is the main cause of chestnut blight—a devastating disease of the American chestnut tree that in the early 1900s caused a rapid, widespread die-off of this once plentiful tree from its historic range in the eastern United States.

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The chestnut blight is a fungal infection affecting the American Chestnut tree that had a devastating economic and social impact on communities in the eastern United States. It later spread to other parts of the world including Italy.[1] The fungus is spread by wind-borne ascospores and, over a shorter distance, conidia distributed by rain-splash action.[2] In the first half of the 20th Century it killed an estimated 4 billion trees. Infection is local in range, so some isolated American chestnuts survive where there is no other tree within 10 km. There are at least two viral pathogens that weaken the fungus through a mechanism termed hypovirulence that helps trees survive.[3][4]

The root collar and root system of the chestnut tree have some resistance to blight infection due to soil organisms adversely reacting to the fungus; consequently, a large number of small American chestnut trees still exist as shoots growing from existing root bases. However, these regrown shoots seldom reach the sexually reproductive stage before being killed by the fungus.[5] They only survive as living stumps, or "stools," with only a few growing enough shoots to produce seeds. This is just enough to preserve the genetic material necessary to engineer an American chestnut tree using genes from any of the disease-immune Asiatic species to confer resistance to the disease.

American chinquapin is also highly susceptible to chestnut blight. The European chestnut and the West Asian species are also susceptible, but less so than the American species. Surviving chestnut trees are being bred for resistance to the blight, notably by the American Chestnut Foundation, which aims to reintroduce a blight-resistant American chestnut to its original forest range within the early decades of the 21st century.[6] The resistant species—particularly Japanese chestnut and Chinese chestnut, as well as Seguin's chestnut and Henry's chestnut—have been used in these breeding programs in the US to create disease-resistant hybrids with the American chestnut.[7] It's important to realize, though, that even Chinese chestnut trees vary considerably in blight resistance. Some individuals are quite susceptible while others are essentially immune to the disease.[8] Many kinds of environmental stress may break down a tree's resistance to blight. Indeed, at higher elevations in areas exposed to severe climate, normally resistant, Oriental chestnuts have been killed by blight.[9] The fungus will also infect other tree species such as oaks, red maples, staghorn sumacs, and shagbark hickories. [10] Once infected, these trees will also exhibit orange bark with cankers. However, they will not exhibit shoot die back and death of the main tree. Instead the pathogen will be able to persist in trees, causing the fungus to be able to attack new growth in American Chestnut trees.

The chestnut blight was accidentally introduced to North America around 1904 when Endothia parasitica was introduced into the United States from Japanese nursery stock.[11] Commonly known as the Chestnut blight, it was first found in the chestnut trees on the grounds of the New York Zoological Garden (the "Bronx Zoo") by Herman W. Merkel, a forester at the Zoo. In 1905, American mycologist William Murrill isolated and described the fungus responsible (which he named Diaporthe parasitica), and demonstrated by inoculation into healthy plants that the fungus caused the disease.[12] By 1940, most mature American chestnut trees had been wiped out by the disease.[13]

Infection of American chestnut trees with C. parasitica simultaneously appeared in numerous places on the East Coast, most likely from Castanea crenata, or Japanese chestnut, which had become popular imports.[14] Japanese and some Chinese chestnut trees have some resistance to infection by C. parasitica: the infection usually does not kill these Asian chestnut species. Within 40 years the nearly four-billion-strong American chestnut population in North America was devastated [15] — only a few clumps of trees remained in California, Michigan, Wisconsin and the Pacific Northwest. Because of the disease, American chestnut wood almost disappeared from the market for decades, although it can still be obtained as reclaimed lumber.[16]

It is estimated that in some places, such as the Appalachian Mountains, one in every four hardwoods was an American chestnut. Mature trees often grew straight and branch-free for 50 feet and could grow up to 100 feet tall with a trunk diameter of 14 feet at a few feet above ground level. For three centuries many barns and homes near the Appalachian Mountains were made from American chestnut.[17]

For the people of the southern Appalachians, the American Chestnut was economically important. The reddish-brown wood was lightweight, soft, easy to split, very resistant to decay; and it did not warp or shrink. Because of its resistance to decay, industries sprang up throughout the region to use wood from the American Chestnut for posts, poles, piling, railroad ties, and split-rail fences.[18] Its straight-grained wood was ideal for building log cabins, furniture, and caskets. The fruit that fell to the ground was an important cash crop. Families raked up chestnuts by the bushels and took wagon loads of them to sell in nearby towns. The people even cooked the chestnuts for their own use. The bark and wood were rich in tannic acid which provided tannins for use in the tanning of leather.[19]

Efforts started in the 1930s and are still ongoing, in Massachusetts[20] and many other places[18] in the United States, to repopulate the country with these trees.[21]

A chestnut tree that has been cut down, with blight on its inner bark and trunk

The fungus enters through wounds on susceptible trees and grows in and beneath the bark, eventually killing the cambium all the way round the twig, branch or trunk.[24] The first symptom of C. parasitica infection is a small orange-brown area on the tree bark. A sunken canker then forms as the mycelial fan spreads under the bark. As the hyphae spread, they produce several toxic compounds, the most notable of which is oxalic acid. This acid lowers the pH of the infected tissue from around the normal 5.5 to approximately 2.8, which is toxic to plant cells. The canker eventually girdles the tree, killing everything above it. Distinctive yellow tendrils (cirrhi) of conidia can be seen extruding in wet weather.[25]

Removing blighted trees to control the disease was first attempted when the blight was discovered, but this proved to be an ineffective solution. Scientists then set out to introduce a hypovirus into the chestnut blight fungus. The trees infected with virus-treated fungus responded immediately and began to heal over their cankers. However, the virus was so efficient at attenuating fungal growth that it prevented spreading of the virus from an infected fungus growing on one tree to that growing on another tree. Only the virus-treated trees recovered. Scientific opinion regarding the future of the stand varies.[26]

Current efforts are under way by the Forest Health Initiative to use modern breeding techniques and genetic engineering to create resistant tree strains, with contributions from SUNY College of Environmental Science and Forestry, Penn State, the University of Georgia, and the US Forest Service. One of the most successful methods of breeding is to create a back cross of a resistant species (such as one from China or Japan) and American chestnut. Researchers identified 2 or 3 genes that allow for blight resistance, and are focusing on giving the American Chestnut hybrids only those genes from the Chinese or Japanese chestnut.[27] The two species are first bred to create a 50/50 hybrid. After three back crosses with American chestnut, the remaining genome is approximate 1/16 that of the resistant tree, and 15/16 American. The strategy is to select blight-resistance genes during the back crossing, while preserving the more wild-type traits of American chestnut as the dominant phenotype. Thus, the newly bred hybrid chestnut trees should reach the same heights as the original American chestnut. Many of these 15/16 American chestnut hybrids have been planted along the East Coast, including in the Jefferson National Forest and on the Flight 93 National Memorial. Some of these sites have had researchers check on the saplings that have been planted to see their survival rate. For the hybrids to do well, they need areas with decent drainage and abundant sunlight.[28] Meeting these needs can be hard to do, so not all restoration areas have been successful with hybrid survival.